1
Department of Nephrology, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
2
Department of Medical Oncology, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
3
Department of Internal Medicine, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
4
Department of Pharmacology, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
5
Department of Histology and Embryology, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
6
Department of Anatomy, Erzincan Binali Yıldırım Üniversitesi, Erzincan, Turkey
7
Department of Biochemistry, Atatürk Üniversitesi, Erzurum, Erzurum, Turkey
Abstract
OBJECTIVE: To show the protective effects of taxifolin on cisplatin-induced oxidative renal injury. STUDY DESIGN: Rats were divided into 3 groups: the healthy group, the cisplatin group (2.5 mg/kg cisplatin only), and the taxifolin-cisplatin group (50 mg/kg taxifolin+2.5 mg/kg cisplatin). The rats were sacrificed after 14 days, and the kidneys were removed for examination of malondialdehyde (MDA), total glutathione (tGSH), and super oxide dismutase (SOD) levels. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood samples taken before the animals were sacrificed. Kidney tissues were examined histopathologically. Finally, biochemical and histopathological results of the groups were compared. RESULTS: Cisplatin significantly increased MDA and decreased tGSH and SOD in the rat kidney tissue (p<0.001). Additionally, cisplatin caused an increase in serum creatinine and BUN levels (p<0.001). Taxifolin prevented the cisplatin-induced increase in MDA and decrease in tGSH and SOD (p<0.001). It also decreased serum creatinine and BUN levels significantly as compared with the cisplatin group (p<0.001). In the cisplatin group microscopic examinations showed obvious kidney damage including dilation, severe necrosis, and degenerative changes. Taxifolin prior to cisplatin markedly ameliorated these changes. CONCLUSION: We have demonstrated for the first time that taxifolin can prevent cisplatin-induced nephrotoxicity. © Science Printers and Publishers, Inc.